title: Organic chemicals in diesel exhaust particles enhance picryl chloride-induced atopic dermatitis in NC/Nga mice.
abstract: BACKGROUND
  Diesel exhaust particles (DEP) have been reported to worsen allergic airway inflammation in mice. Recently, the organic chemical components of DEP (DEP-OC) were found to be important contributors to the aggravation of allergic airway inflammation in mice. The purpose of this study was to examine the effects of DEP-OC on atopic dermatitis (AD)-like skin lesions induced by picryl chloride (PiCl) in NC/Nga mice.
  
  
  METHODS
  DEP were extracted with benzene/ethanol, and the soluble organic fraction formed the DEP-OC. NC/Nga male mice received simultaneous application of DEP-OC and/or PiCl on their ears once a week for 9 or 3 weeks. We evaluated skin lesions by noting scaling, eruption, excoriation, erosion, hemorrhage, pathologic changes, production of cytokines, and IgE level in the serum.
  
  
  RESULTS
  PiCl application alone produced progressively severe AD-like skin lesions. The application of PiCl plus DEP-OC resulted in a marked worsening of skin lesions in the early stages of AD. Moreover, mast cell counts significantly increased in the subcutaneous tissue. Administration of PiCl combined with DEP-OC resulted in a greater increase in the local expression of interleukin-4, keratinocyte chemoattractant, and neutrophils in subcutaneous tissue compared with PiCl treatment alone. In contrast, the combination treatment produced lower levels of IFN-γ compared with PiCl treatment alone.
  
  
  CONCLUSIONS
  DEP-OC application to the skin aggravated PiCl-induced AD. This aggravation may be due to activation of the Th2-associated immune responses by the organic chemicals in DEP.
authors.affiliation: Department of Health Sciences, Oita University of Nursing and Health Sciences, Oita, Japan.
authors.forename: Kaori
authors.initials: K
authors.lastname: Sadakane
authors.forename: Takamichi
authors.initials: T
authors.lastname: Ichinose
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Takano
authors.forename: Rie
authors.initials: R
authors.lastname: Yanagisawa
authors.forename: Ken-ichiro
authors.initials: K
authors.lastname: Inoue
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Kawazato
authors.forename: Aiko
authors.initials: A
authors.lastname: Yasuda
authors.forename: Kazuichi
authors.initials: K
authors.lastname: Hayakawa
mesh_terms: D000818:Animals; D003876:Dermatitis, Atopic / Q000139:chemically induced* / Q000276:immunology / Q000503:physiopathology*; D004195:Disease Models, Animal; D005786:Gene Expression Regulation / Q000187:drug effects; D008297:Male; D008407:Mast Cells / Q000187:drug effects; D051379:Mice; D009930:Organic Chemicals / Q000633:toxicity*; D010853:Picryl Chloride; D012867:Skin / Q000187:drug effects*; D001335:Vehicle Emissions / Q000032:analysis / Q000633:toxicity*
chemical_list: D009930:Organic Chemicals; D001335:Vehicle Emissions; D010853:Picryl Chloride